Thursday, March 15, 2012

Genopolitics: Evan Charney's Response

In response to my post on Evan Charney's critique of genopolitics and the genetic paradigm, he has sent me the following reply, which I am reproducing in full:

Larry: I appreciate your blog comments and your careful and insightful reading of my paper for Brain and Behavioral Sciences Let me attempt to respond to a few of your remarks regarding the APSR paper.

One thing I would like to highlight in reference to that article is that the same two genes that Fowler and Dawes associated with voting have been associated with every conceivable behavior (and a large number of non-behavioral traits). Readers should look at the following updated version of Table 2:

A specific polymorphism of the MAOA gene has been associated with, among other things, agreeableness, alcoholism, Alzheimer’s disease, anger/aggression, anorexia nervosa, antisocial behavior, attention deficit hyperactivity disorder, attitudes toward longshot risks, auditory evoked potentials, binge drinking, bipolar disorder, bulimia, bone mineral density, borderline personality disorder, chronic fatigue syndrome, conscientiousness, contraception use, cooperativeness, credit card debt, depression, educational continuation, extraversion, facial expressionrecognition, fearfulness, fibromyalgia, gambling, gout, hypertension, insomnia, intelligence, memory, narcolepsy, neuroticism, novelty seeking, openness, pain perception, panic disorder, Parkinson’s disease, persistence, restless legs syndrome, reward dependence, schizophrenia, smoking, social phobia, stress response, success by Wall street professionals, sudden infant death syndrome, temperomandibular disorder, time perception, and Tourette syndrome.

What is going on is data mining on a massive scale: A number of large data sets contain the same polymorphisms of the same five or six genes, with the result that these genes have been associated with every imaginable trait (and for everystudy showing an association, there is another study showing no association).

Regarding the unfortunate terms “genetic determinism” v. “environmental determinism”: The issue from the standpoint of genetics concerns whether or not specific variations in specific polymorphisms contribute to variations in complex human behaviors in such a manner that we can say that the polymorphism is associated with, and presumably plays a causal role in, variation in the behavior in question.

Political behavior and personality are not like cystic fibrosis and sickle cell anemia, i.e. they are not monogenic disorders in which a mutation in a single gene results in the transcription of an abnormal protein that plays a key role in certain metabolic processes and results in the disorder in question.

What we now know of what falls under the rubric of “behavior” is as follows. The most advanced studies concern fruit flies because research allows for kinds of investigation not possible in humans: Variation in anger involves variation in proteins encoded in thousands of genes, with extensive pleiotropy and epistasis (i.e., non-additivity). I particularly recommend Zwarts, et al. 2011. "Complex genetic architecture of Drosophila aggressive behavior." Proceedings of the National Academy of Sciences 108 (41):17070-5. Plasticity means that there is no single route to variation in aggression on the molecular, physiological, and environmental level.

"Genes" v. "environment" is a false dichotomy (but saying this in no way implies that polymorphisms can predict complex behavior). The gene after all, has to be transcribed, and once we acknowledge that then we are going to need to know, e.g., cellular/physiological factors influencing the transcription of the gene (e.g., epigenetic state of the gene to be transcribed), what cellular physiological factors influence which form of agiven protein synthesized by the cell from the gene (e.g., alternative splicing), what processes influence the manner in which that protein is transferred out of the cell in which it is produced, what homeostatic mechanisms regulate the relevant protein at the relevant level in the relevant tissue (e.g., even if a polymorphism does enable “faster transcription” of a protein by the cell, that in no way automatically translates to more of that protein, since homeostatic mechanisms may serve to counteract any perceived protein or hormonal imbalances. All of these are environmental processes, but the structure of a gene is so intertwined with all of the biological-environmental processes involved in its transcription, translation, and ultimate physiological effect, that the dichotomy gene-environment is a false one.

Every advance in molecular genetics indicates an extraordinary conservation of the genome of species, including plants (corn as noted in the article, has more genes than humans). The key differentiating factor between species is the processes that regulate gene transcription. These facts are a game changer.

We simply cannot predict from the structure of a polymorphism what effect (if any) it is going to have, or is likely to have, on behavior. This is what I mean by "genetic determinism," a perhaps unfortunate usage. All of this is argued at greater length from the perspective of genetics, neurobiology, and evolutionary theory in “Behavior Genetics and Post Genomics,” forthcoming in Behavioral and Brain Sciences.


I suggest that Rebecca Hannagan read this piece carefully and I would be happy to discuss it with her

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